Open Access

Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa‑miR‑542‑3p

  • Authors:
    • Zhen Jia
    • Yadong Wang
    • Xiaoya Sun
    • Xuefeng Zhao
    • Yan Zhang
    • Shuangyan Xu
    • Yisheng Wang
    • Yuebai Li
  • View Affiliations

  • Published online on: July 15, 2021     https://doi.org/10.3892/ol.2021.12930
  • Article Number: 669
  • Copyright: © Jia et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Cancer cells use glucose via glycolysis to maintain tumor cell proliferation. However, the effect of long non‑coding RNAs (lncRNAs) on glycolysis in osteosarcoma (OS) cells remains unclear. The present study aimed to investigate the involvement of the lncRNA XLOC_005950/hsa‑microRNA (miR)‑542‑3p/phosphofructokinase, muscle (PFKM) axis in the regulation of glucose metabolism, cell proliferation and apoptosis in the progression of OS. lncRNA XLOC_005950, hsa‑miR‑542‑3p and PFKM expression in OS tissues and cells was detected via reverse transcription‑quantitative PCR analysis. CRISPR/Cas9 gene editing was used to knockout lncRNA XLOC_005950 expression in MG63 cells. Cell Counting Kit‑8 assay, flow cytometry, PFKM activity, and glucose and lactic acid content determination were performed to assess the effects of lncRNA XLOC_005950 knockout and overexpression of hsa‑miR‑542‑3p on the phenotypes of OS cells. The dual‑luciferase reporter assay was performed to confirm the targeting associations between lncRNA XLOC_005950, hsa‑miR‑542‑3p and PFKM. The results demonstrated that lncRNA XLOC_005950 expression was upregulated in OS tissues and cells. Functional experiments indicated that lncRNA XLOC_005950 knockout decreased PFKM activity, the intracellular glucose and lactic acid content, and cell proliferation, while increasing apoptosis of OS cells. Furthermore, lncRNA XLOC_005950 knockout upregulated hsa‑miR‑542‑3p expression and downregulated PFKM expression. Overexpression of hsa‑miR‑542‑3p suppressed PFKM expression. Furthermore, lncRNA XLOC_005950, as the molecular sponge of miR‑542‑3p in OS, modulated the downstream target gene, PFKM. Taken together, the results of the present study suggest that lncRNA XLOC_005950 knockout may inhibit the progression of OS via hsa‑miR‑542‑3p‑mediated regulation of PFKM expression.
View Figures
View References

Related Articles

Journal Cover

September-2021
Volume 22 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Jia Z, Wang Y, Sun X, Zhao X, Zhang Y, Xu S, Wang Y and Li Y: Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa‑miR‑542‑3p. Oncol Lett 22: 669, 2021
APA
Jia, Z., Wang, Y., Sun, X., Zhao, X., Zhang, Y., Xu, S. ... Li, Y. (2021). Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa‑miR‑542‑3p. Oncology Letters, 22, 669. https://doi.org/10.3892/ol.2021.12930
MLA
Jia, Z., Wang, Y., Sun, X., Zhao, X., Zhang, Y., Xu, S., Wang, Y., Li, Y."Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa‑miR‑542‑3p". Oncology Letters 22.3 (2021): 669.
Chicago
Jia, Z., Wang, Y., Sun, X., Zhao, X., Zhang, Y., Xu, S., Wang, Y., Li, Y."Effect of lncRNA XLOC_005950 knockout by CRISPR/Cas9 gene editing on energy metabolism and proliferation in osteosarcoma MG63 cells mediated by hsa‑miR‑542‑3p". Oncology Letters 22, no. 3 (2021): 669. https://doi.org/10.3892/ol.2021.12930